Хирургические болезни. Практикум = Surgical diseases. Practice book. Учебное пособие

•microvascular transplantation of the epiploon on the shin (I.I. Zatevakhin et al., 1983);

•autotransplantation of soft-tissue flaps to the shin (foot / thigh) (V.G. Samodai, 2003);

•arterial veins of the lower leg and foot (A.V. Pokrovsky, 1996). Performed in “critical ischemia” or in case when it is impossible to conduct a standard reconstructive surgery by forming an anastomosis of the shin veins with the popliteal or tibial arteries;

•revascularizing osteotrepanation of the shin bones (O.P. Kazanchyan, 1996) – involves application of pointing trepanation holes in the diaphysis of the tibia, which is then followed by the opening of extremity reserve capillaries.

The presented operations are contraindicated for prolonged occlusions of vessels or if ischemic edema and purulent-necrotic tissue changes are observed.

3. Minimally invasive (X-ray endovascular) interventions.

They are performed most often in patients of elderly, senile age due to the lack of opportunities for reconstructive interventions, or with repeated occlusions of vessels (after the already performed endarterectomy). They include:

•transluminal balloon angioplasty (more often, this procedure is used for stenoses of the femoral and iliac arteries) (A. Gruentzig, 1974);

•endostenting (endoprosthetics) of the femoral, popliteal and tibial arteries through transcatheter angioplasty.

2.4. NONSPECIFIC AORTO-ARTERITIS

Nonspecific aorto-arteritis (NAA) (synonyms: Martorel’s syndrome, panaarietitis, aortic arch syndrome, Takayasu’s disease) represents a systemic segmental autoimmune disease accompanied by stenosis of the aorta arch and the major arteries. It occurs more often in women aged 20–40.

Etiology. The etiological factors of NAA are:

•autoimmune diseases that promote the increase in the titer of antibodies to cardiolipid (or antiphospholipid), specific antimedial and anti-aortic antibodies IgG (their main localization is the aortic arch), IgM and CIC (localized predominantly in the muscle layer and in the places of the major arteries elastic fibers destruction);

•genetic predisposition to the inheritance of certain histocompatibility antigens (HLA): B-39; B-52; DR-B1;

•inflammatory diseases, accompanied by a productive process, bacterial infection, as well as mycoses, chlamydial infection, syphilis;

•collagen dysplasia (syndrome Ehles-Danlos TMh IV type).

Classification. Clinically four types of NAA are currently distinguished, taking into account the prevalence of the process:

•I – isolated type of lesion of the aorta arch;

•II – lesion of the thoracovisceral segment of the aorta, including vis-

ceral branches and renal arteries;

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•III – mixed type (includes changes in types I and II);

•IV – any of the previously presented options involving the branches of the pulmonary artery.

2.5. OBLITERATING THROMBOANGIITIS

Obliterating thromboangiitis (OTp) is a chronic inflammatory systemic vascular disease caused by occlusive lesions of arteries, veins of small and medium diameter, accompanied by a distal ischaemia of the limb on the background of an autoimmune component. It constitutes about 0.5−2% of all ODLEV and occurs mainly in men (98% of cases) aged 30–50 years (80% of cases).

This disease, being known since ancient times, had different names: Raynaud-Friedlander’s disease; Vinivarter-Burger disease, “spontaneous gangrene”, and until 1955 it was more commonly known as “obliterating endarteritis”.

Characteristic features of OTp are:

•systemic pathology of the vessels – arteries and veins of a small, rarely medium, diameter of the ascending character. In 12–75% of cases, the vessels of the upper and lower extremities are affected, of which in 72–86% of occlusion cases of the abortion segment are observed, in 6% – of the ile- um-femoral segment. Very seldom (in 10% of cases) coronary arteries, and in 7% of cases carotid arteries are involved;

•recurrencies are observed in 15–40% and have the pattern of “migrating” thrombophlebitis of deep veins;

•inflammation is predominantly localized in the subendothelial layer of the arteries on the background of a general hyper-autoimmune reaction of the body;

•microscopically the following features prevail: vascular hyperemia, spasm, hemorrhage, migration of monocytes and lymphocytes first to the vascular wall, and then to periarticular tissues;

•absence of microbial pathogen;

•involvement of the entire vascular system (less often – concentration in only one organ or in one place) in the hyperergic reaction.

Clinical picture. OTp proceeds both in the subacute and recurring form with the appearance of “migrating” phlebitis of superficial (more rarely deep) veins, combined with spasm, occlusion and chronic arterial ischemia of the extremities. It is accompanied by a periodic alternation of remission and new exacerbations involving new parts of the arterial system. Rarely in OTp a type with gradually progressing course, phenomena of critical ischemia and ulcerative-necrotic manifestations can occur.

The classic sign of OTp is complete obliteration of the deep femoral artery (DFA) along the whole way while maintaining the patency of the superficial femoral artery.

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Chapter 3

VASCULAR DISEASES.

DISEASES ACCOMPANIED BY IMPAIRED

VENOUS DRAINAGE

3.1. ACUTE VENOUS INSUFFICIENCY

Acute venous insufficiency (AVI) is a symptomatic complex of sudden disturbances of venous return due to various causes.

The main cause of AVI is venous thrombosis, less often – compression of the venous lumen from the outside due to hematoma, trauma or intraoperative dressing of large venous trunks.

Venous thrombosis (VT) is the process of intravital occurrence of a thrombus in the lumen of the veins of different localization (systems of the superior vena cava and inferior vena cava).

Clinically, the following notions are distinguished: phlebothrombosis, it is the process of deep vein thrombosis, and thrombophlebitis, it is thrombosis localized in the subcutaneous (superficial) veins.

VT localized in the veins of the lower leg (tibia) is called peripheral and the one localized in the ileo-caval segment is called central. In terms of pathogenesis, the difference between phlebotrombosis and thrombophlebitis exists only in the initial stage of the process, during the first 2−3 days, when the thrombus is located in the part of the initially unaltered venous wall and is not sufficiently attached to it, thus causing a high risk of developing pulmonary embolism. In the future, these differences disappear, because when a thrombus is being formed, inflammatory reactions in the endothelium of the vein with the development of phlebitis are activated.

“Varicothrombophlebitis” is a notion that denotes thrombophlebitis in the system of varicose subcutaneous veins.

Classification. Clinically, the following classification of VT is used:

•thromboses in the system of the superior vena cava (SVC), interpreted as stress thromboses (make up about 1–5% of all VT) are subdivided by localization:

surface vein systems (thrombophlebitis of the main and cephalic veins of the arm, external jugular veins, and thoracic wall veins);

deep veins (synonym for Paget-Schroetter syndrome) – superior vena cava, innominate vein, jugular vein, subclavian vein, axillary vein, shoulder and forearm veins);

•thrombosis in the system of inferior vena cava (IVC) account for more than 95% of all VT cases. They are subdivided by location into VT of:

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deep veins (lower leg, hip and retroperitoneal space, i.e. iliac, renal, gonadal, hepatic, IVC);

superficial veins (thrombophlebitis of large or small saphenous veins (GSV / SSV), veins of the anterior abdominal wall);

perforating veins (lower leg and hip);

•according to the nature of thrombosis, the following types are distinguished:

ascending (extending from the distal segments of the venous system to the proximal ones);

descending (extending from the proximal to the distal segments);

simultaneous (occurs simultaneously in the veins of different extremities or various venous basins);

bipolar (occurs at different levels of the same venous basin);

occlusive (completely blocks the venous return);

nonocclusive (partially blocks the lumen). It may be:

−floating, when the bottom of the thrombus is in the vein area and is attached to the vein at one point, while the upper part of it

spreads intravenously and floats freely in the blood stream at a rather considerable distance (frequently more than 15−20 cm), so there is a high probability of fragmentation of the thrombus and subsequent embolization;

−mural, when the thrombus is tightly attached to the venous wall due to pronounced phlebitis;

segmental (localized in one segment of the venous wall);

widespread;

•according to the severity of hemodynamic disorders in the extremity (only for deep vein VT), we distinguish:

mild;

moderate;

severe disorders, following the pattern of phlegmasia cerulia (or venous gangrene) and phlegmasia alba;

•according to complications:

pulmonary embolism (PE);

venous gangrene;

post thrombotic syndrome (PTS).

Etiology. In the VT etiology, the emphasis is made on R.Virchow’s classical triad (1856), consisting of:

•damage of the venous wall;

•retardation (interruption) of venous return by 2−3 times;

•changes in the blood aggregation properties (mainly due to the activation of coagulation and thrombus formation).

The factors causing VT include:

•prolonged bed regime, long plaster or other immobilization of the extremity; forced position (including “Economy Class” flights);

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•trauma of the venous wall due to broken bones of the lower leg, thigh, pelvis, or stab wounds);

•congenital factors (due to inadequate synthesis of antithrombin III and proteins S and C);

•hormonal contraceptives, smoking (both increase the VT risk more than 7 times).

Clinical picture. Clinically, deep vein thrombosis of the lower leg (peripheral phlebothrombosis) is manifested:

•in incomplete occlusion of the lumen – by unpronounced pain in the calf muscles, which increase with walking or prolonged stay in an upright position (more often by the end of the day);

•by edema of the foot, ankle joint and lower third of the leg (as compared to the healthy leg) by 2−3 cm;

•by local temperature increase;

•by skin cyanosis.

Among the specific symptoms indicative of deep vein thrombosis and determined only during the first 24 hours since the beginning of the process, there are:

•Homans-Mayer’s sign – the appearance of pain in calf muscles on maximum dorsiflexion of the foot;

•Moses’ sign – the appearance of pain on compression of the calf muscle forwards against the tibia;

•Lowenberg’s sign – the sign is positive when pain is elicited rapidly

when a blood pressure cuff (of the Korotkov sphygmomanometer) is placed around the calf and inflated to 60−150 mm Hg (on the healthy leg pain appears only after 180 mm Hg).

Thrombosis of the common femoral vein (CFV) is manifested by:

•quick-spreading (bottom-up) edema of the lower leg and thigh within 24 hours;

•skin cyanosis intensifying in a distal direction;

•intensified venous subcutaneous pattern;

•local and general body temperature increase (up to 37 °C);

•accompanying secondary lymphangeitis and lymphadenitis.

Thrombosis of the ileum-femoral segment (ileofemoral phlebothrom-

bosis) occurs in the form of two clinical stages:

•prodromal (or initial) stage manifested by pain syndrome on the affected side, less often in the lumbosacral region, elevated body temperature to a febrile level;

•expressed clinical manifestations characterized by:

pronounced severe pain and a feeling of fullness in the extremity;

edema of the leg from the inguinal fold up to the scrotum junction, gluteal region and lower parts of the anterior abdominal wall.

In especially severe cases, the course of ileofemoral phlebothrombosis is complicated by:

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•phlegmasia alba dolens, also called a pseudoembolic form due to the arterial spasm of the homonymous artery associated with phlebothrombosis. Its manifestations include pain, numbness and coldness of the extremity, disappearance of peripheral pulsation, milky or pale blue color of the skin in the setting of the marked edema of the extremity;

•phlegmasia coerulea dolens, a synonym for Gregoire’s disease. The manifestations include marked edema of the entire affected leg with the cyanosis of the skin and local dilation of the subcutaneous veins and capillaries (“marble” color) with the associated sharp pain syndrome and coldness of the extremity.

In a number of cases, this complication of VT, due to the occlusion of the main veins and peripheral collaterals, leads to the temporary development of acute arterial insufficiency (AAI) with the overflow of arteriolovenous shunts. In the case of venous gangrene, there appears skin necrosis, as well as clinical features of hypovolemic shock due to the deposition in the affected extremity of up to 4 liters of blood) and thereafter, signs of endogenous intoxication develop.

Diagnosis. Diagnosis of VT includes:

•ultrasound – duplex angioscanning of veins in the color duplex imaging (CDM) mode, which allows to specify the localization and character of venous occlusion;

•retrograde radiopaque ileocavagraphy;

•spiral CT – and nuclear magnetic resonance imaging – phlebography;

•scintigraphy with fibrin labeled radioisotope Technetium-99;

•assessment of hemocoagulation disorders by determining the level of AT-III; Protein C and S; D-plasma dimers and APTT index.

Treatment. The surgical treatment of VT is used in cases of a high risk of PE developing at suspicion on phlegmasia cerulea. For this they use:

•open thrombectomy with recanalization of venous outflow and subsequent formation of temporary arteriovenous fistulas for a period of 3–6 months;

•ligation of the main veins (superficial, femoral, iliac);

•IVC plication with the help of special staplers;

•endovascular interventions (including implantation of a cava filter, catheter indirect endovascular thrombectomy from IVC or iliac veins, catheter thrombolysis).

3.2. CHRONIC VENOUS INSUFFICIENCY

Chronic venous insufficiency (CVI) is a pathological complex of symptoms gradually developing venous outflow disorders accompanied by local trophic tissue disorders.

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The main causes of CVI include:

•varicosis of the veins of the lower extremities (VLE);

•secondary changes of veins, caused by deep vein thrombosis with the development of post-thrombophlebitic disease (PTD);

•decompensated heart failure.

Varicose disease (VD) is a disease of the veins of the lower extremities (LE) due to a persistent and irreversible change in their lumen, length and changes in their valvular apparatus. Among the transformations of the venous wall, the sac and zig-zag formation, cylindrical and mixed types of changes are distinguished.

Depending on the pathogenesis, there is primary varicosis due to changes in the properties of the venous wall, and secondary varicosis caused by the development of PTD or congenital anomalies (most frequently – functioning arterio-venous fistulas, or congenital occlusion of tibial veins).

Classification. VD is classified by:

•localization of the lesion:

in the system of a large saphenous vein (LSV);

in the system of a small saphenous vein (SSV);

in both venous pathways;

atypical (on the lateral or posterior surface of the thigh, perineum). In locating the lesion the extremity is indicated (left, right, or bilateral

lesion).

•localization of venous reflux:

saphenofemoral anastomosis / junction;

saphenopoplite fistula;

perforated femoral veins;

perforated tibial veins;

deep veins;

•according to CEAP classification:

Class 0 (C0): no visible and palpable signs of venous disease;

Class 1 (C1): telangiectasis of reticular veins;

Class 2 (C2): presence of varicose veins;

Class 3 (C3): edema;

Class 4 (C4a): pigmentation or eczema;

Class 4 (C4): blipodermatosclerosis or athrophie blanche;

Class 5 (C5): healed venous ulcers;

Class 6 (C6): active venous ulcers;

•severity of CVI:

0 degree – absent;

I degree – transient edema of the tibia or ankle joint;

II degree – persistent edema, hyperpigmentation, lipodermatosclerosis, cellulitis;

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III degree – open or healed trophic ulcer;

•complications:

arrosive bleeding from a varicose transformed wall;

varicothrombophlebitis (thrombosis at the site of a varicose vein);

trophic ulcer.

Etiology. The etiology of VLE is due to a combination of causes, among which the most important ones are:

•heredity – due to genetic factors contributing to the weakness of the connective tissue, the synthesis of type I collagen increases, which enhances the rigidity of the wall, the production of type III collagen responsible for increasing the elasticity of the wall decreases. Genetic factors are combined with the development of hernia of the anterior abdominal wall, hemorrhoid, flatfoot and myopia. In the presence of VD in both parents – the risk of inheritance of the disease in children rises up to 85%;

•insufficiency of venous valves (primary and secondary) leading to the loss of their functions;

•female gender (occurs 4 times more frequently than in men), age (occurs in 70% of patients over age 65–70);

•pregnancy and multiple births;

•increased hydrostatic pressure (typical for occupations characterized by prolonged stay on legs or in forced sitting position);

•decreased function of the muscular-venous pump;

•musculoskeletal system disorders (presence of flat feet, scoliosis and valgus deformation in the medical history).

Treatment. Operative treatment of VD includes three main directions:

•elimination of cosmetic defect;

•elimination of CVI symptoms;

•prevention of complications.

The main indications for surgical treatment are:

•saccular or mixed transformation of the venous wall with an increase in the external diameter of the vein over 11 mm;

•the presence of complicated forms of VD (Class 4 and higher according to CEAP);

•signs of valvular failure with the development of vertical and / or horizontal reflux.

Surgical interventions in VD include:

1. Operations on superficial varicose veins:

•traditional combined phlebectomy. It is performed by isolating, crossing and bandaging / ligating the orifice of LSV (this stage is called TroyanovTrendelenburg operation or a crossectomy), followed by removal of LSV and SSV trunk using special flexible or rigid probes (this intervention is called stripping or Babcock operation). When it is performed, two options are possible: removal of the LSV on the femur and tibia (long stripping) or

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only on the femur or only on the tibia (short stripping). Separate varicose LSV-SSV branches are removed by means of additional incisions on the tibia or femur (Narat’s technique) or by puncturing the skin with the removal of the vein sections with the help of a special set of hooks or Varadi / Mueller extractors (mini-phlebectomy);

•endovascular laser coagulation (EVLC). It is carried out by athermal action on the endothelium of the vein (vaporization of its intima) followed by the formation of intraluminal thrombus and fibrosis. EVLC can be performed either by puncture of the vein under ultrasound control or by means of Troyanov-Trendelenburg access. It is indicated in the rectilinear course of venous trunks up to 10 mm in diameter, cosmetic removal of intradermal veins and telangiectasies;

•endovasal destruction by “gluing” or freezing the endothelium of the venous trunk of LSV / SSV and / or their ducts to a special cryoprobe, cooled as low as 190 o (Celsius);

•transdermal or catheter sclerotherapy by intravenous administration of special drugs that cause obliteration of the venous lumen (thrombovar, varicocide, variglobin, fi bro-vein, ethoxysclerol or various microgenic preparations). It is used to treat varicose disease of Class 1 and 2 when drugs are introduced into the lumen in the form of a nonjagged substance in case of limited (intradermal) varicosis or telangiectasies as well as in case of relapses in individual subcutaneous veins. It is contraindicated in the presence of horizontal and vertical venous reflux.

2. Operations for the removal of perforated veins include interventions by means of:

•subfascial access: subfascial ligation of the tibial perforated veins by an operation of the Linton type (Felder), endoscopic dissection with the separation of the perforated veins by clipping them (electrocoagulation) with the help of special endoscopic equipment and instruments;

•epifascial access: suprafascial (open) ligation of individual perforated veins by means of incisions on the skin (Cockett’s technique) or with the help of a set of Müller or Varadi hooks or special tools – Tri Vex – a resector under ultrasound control.

3. Operations to correct the valvular apparatus of deep veins which are performed in 3–5% of patients with C-5-C-6 class and are combined with disorders of deep veins valves include closed types of interventions on the valves:

•concentric narrowing of their lumen from the inside (A.N. Vedensky’s technique) with the help of a wire spiral, or by introducing a section of a previously removed autovein into the lumen;

•extravasal valvuloplasty by tying a special suture on the side of the vein adventitia, involving the damaged venous valve layer.

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3.3. POST-THROMBOPHLEBITIC DISEASE

Post-thrombophlebitic disease (PTD) (synonyms: post-thrombotic disease, post-thrombophlebitic syndrome) is a disease of the venous system, which is the outcome of previous acute VT (8–9 months before). It is manifested by CVI signs and develops in 2−3% of the entire adult population or in 10% of patients with CVI.

Classification. PTD is classified by:

•the prevalence of clinical symptoms:

swelling and pain;

varicose veins (secondary varicosis);

ulcerative;

mixed type (includes all 3 listed components);

•the outcome of the process:

recanalization (full or partial);

occlusion (secondary obliteration of the venous lumen);

mixed type;

•localization of the process (in the venous segment):

IVC;

the iliac segment;

the femoral segment;

popliteal segment;

tibial veins;

•the character of complications occurring as:

arrosive venous (external) bleeding;

trophic disorders (hyperpigmentation of the skin, lipodermatosclerosis, trophic ulcers);

varicothrombophlebitis or purulent peliphlebitis;

•class of CVI (see CEAP classification).

Treatment. Treatment of PTD consists of:

Conservative stage including:

•application of constant (round the clock) medical compression stockings of II–III class, which provides the pressure of 34–46 mm Hg at the level of the ankles;

•phlebotonics (preparations improving venous drainage): detralex, phlebodia, cyclo-3-fort, antistax, escus, troxerutin;

•drugs that improve microcirculation and cellular metabolism in tissues. Surgical stage, carried out in the presence of complicated forms by

means of:

•phlebectomy of the repeatedly altered subcutaneous veins (after complete restoration of the patency of deep veins);

•cross femoral-femoral bypass (Palm-Desperone operation) – performed in case of unilateral complete occlusion of the ileum vein by artificially creating a new way of venous drainage from the affected leg along the newly created shunt, formed in the suprapubic region from a healthy limb.

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